1. Field of the Invention
This invention relates generally to a dietary therapeutic supplement for increasing the production or turnover of serotonin within the brain, thereby decreasing or eliminating pain, depression, and other undesirable physiological conditions. The invention particularly relates to a composition which promotes the transport of both bound and unbound tryptophan from the blood into the brain where tryptophan is converted into the neurotransmitter serotonin.
2. Description of Prior Developments
Attention has recently turned to nontraditional methods and compositions for treating various physiological disorders in an effort to provide relief in those instances where standard techniques have proven ineffective and where it is desired to avoid the drawbacks of conventional pharmaceuticals. More particularly, attention has turned to new methods and compositions for treatment of pain, depression, insomnia and appetite control.
One approach has been to attempt to relieve such conditions through dietary supplementation of L-tryptophan (tryptophan). Once within the brain, neurons convert tryptophan into the neurotransmitter serotonin. It has been found that an increase of tryptophan in the brain increases the brain's production of serotonin. The level of serotonin within the brain has been shown to be linked to sleep, appetite, depression and pain threshold. Disturbances in the brain causing reduced levels of serotonin have been linked to clinical depression, insomnia, and lowered pain threshold. The latter abnormality results in chronic, intractable pain.
It is known that dietary supplementation of tryptophan increases the level of tryptophan within blood plasma and facilitates the passage of tryptophan across the blood-brain barrier into the brain. The increased amount of tryptophan in the brain permits a greater amount of tryptophan to be converted to the neurotransmitter serotonin.
The level of one's pain threshold, a mechanism that normally prevents the brain from interpreting stimuli below a certain level as pain, is directly related to the amount of serotonin that is present in the brain. The higher the level of serotonin that is present, the higher will be the pain threshold level, up to a normal maximum level. With normal amounts of serotonin, one can function in a normal manner and not be subjected to myriad stimuli (such as from muscle activity) that could be interpreted as pain impulses. Moreover, clinical depression and insomnia can also be relieved by increasing serotonin production within the brain, up to a normal level.
In order for tryptophan to be converted to serotonin in the brain, it must cross a separating mechanism that exists between the bIood vessels and the brain. To reach the brain, tryptophan requires a carrier transport mechanism which literally carries tryptophan across this very selective blood-brain barrier into the brain. Because of its polar nature, tryptophan requires a carrier protein to transport it across the blood-brain barrier. Not only is tryptophan carried by this transport mechanism, but other selected amino acids, called large electrically neutral amino acids (LNAAs), are carried as well. Tryptophan not only has to compete with these LNAAs for access to the transport carrier mechanism, it also has a lower affinity for the carrier system than does the LNAAs. To compound this biased situation further, tryptophan in foods is generally present in lower amounts than the LNAAs--particularly in animal proteins. All of these factors contribute to limit the amount of tryptophan that gets through to the brain, to be finally converted into serotonin.
There are numerous conditions, improper diet constitutes one of them, that can interfere with and decrease the amount of tryptophan that normally passes through the blood-brain barrier into the brain each day. This comes about when the ratio of tryptophan to LNAAs in the blood going to the brain is lower than normal. This means that the number of molecules of tryptophan present at the blood-brain barrier is much smaller than the number of LNAAs present at the same blood-brain barrier. The LNAAs outnumber and overwhelm the tryptophan by monopolizing most of the transport carriers. Accordingly, very little tryptophan is provided passage into the brain, compared to the number of LNAAs that are provided passage.
In attempting to correct this improper tryptophan/LNAA ratio, it was found that increasing the total protein intake (obtained from normal dietary sources) in order to add more tryptophan to the system paradoxically results in an even greater decrease in the pain threshold level. This is so because there are usually more LNAAs than there is tryptophan in food. Experimental studies have established the fact that increasing the amount of protein as food, in order to improve the tryptophan/LNAA ratio, only makes the tryptophan/LNAA ratio worse because of the greater intake of the LNAAs over the intake of the tryptophan.
With less tryptophan getting into the brain, less serotonin is formed, and the pain threshold is lowered to the point where low level sensory perceptions which would have been filtered out by the normal pain threshold level are now interpreted by the body as pain stimuli and are experienced as pain. This pain can span the gamut from relatively insignificant annoyances to chronic, unremitting, intractable, excrutiating pain. Because this type of pain stems from a biochemical imbalance involving the tryptophanserotonin relationship which cannot be corrected by any medication, it is unmanageable by any conventional drug therapy--because the drug does not address itself to the correction of this specific biochemical imbalance. The same is true in the case of clinical depression, insomnia and several appetite-related disorders. Conventional therapy for these conditions typically does not consider or correct a possible serotonin deficiency.
Accordingly, a need exists for a method and composition for transporting an effective dose of tryptophan across the blood-brain barrier into the brain and for promoting the conversion of tryptophan into serotonin in order to relieve pain, depression, insomnia and other undersirable physiological conditions.